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MHD2 Neuro > Exam 2 Pathology > Flashcards

Exam 2 Pathology Flashcards

1
Q

Radicular pain

A

aka Root Pain

Lightning, stabbing, shooting pain in the dermatomal distribution of a dorsal root. Result of inflammation or extramedullary compression of a dorsal root.

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2
Q

What is Transection/Transverse Myelopathy?

Describe the etiology (4) and general presentation (3)

A

Refers to a complete or nearly complete lesion encompassing the cross-sectional extent or breadth of the spinal cord at one, or a few adjacent, levels.

Etiology: Trauma, inflammation, compression, ischemia

Presentation:

  1. LMN signs localized to level of lesion
  2. UMN signs in limb muscles below level of lesion
  3. May present w/ septic shock
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3
Q

Describe the etiology, pathophysiology and presentation of Syringomyelia

A

Pathophys: Cavity (syrinx) in central gray matter, which can expand.

Presentation: Initial vest-like spinothalamic sensory loss (pain/temp), w/ sacral sparing and sparing of positon sense/ vibration sense. Can have LMN signs if cavity disrupts anterior horn cells.

Etiology:

  1. Abnormal CSF flow/pressure due to Chiari malformations
  2. Tumor
  3. Residual from trauma
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4
Q

Arnold-Chiari malformations

A

Downward displacement of the cerebellar tonsils through the foramen magnum (the opening at the base of the skull), sometimes causing non-communicating hydrocephalus as a result of obstruction of cerebrospinal fluid (CSF) outflow.

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5
Q

Describe the presentation of Occlusion of the Anterior Spinal Artery

A

Sudden hyperreflexic, spastic paraparesis, loss of pain and temp below the lesion level.

Preserved vibration and position sense (intact dorsa columns).

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6
Q

Describe the etiology (3), pathophysiology and presentation of Subacute Combined Degeneration of the Spinal Cord

A

aka Posterolateral Syndrome

Pathophys: Lesions in the posterior and lateral columns, usually at the thoracic level

Presentation: Loss of vibration and position sense in lower limbs (pain/temp preserved).

UMN signs (due to CST lesion) in lower limbs

Etiology: B12 deficiency* (most common), copper deficiency, HIV

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7
Q

Describe the etiology, pathophysiology and presentation (3) of Tabes Dorsalis

What is also seen in conjunction with this disease?

A

Pathophys: Dorsal root lesions followed by subsequent dorsal column degeneration

Presentation:

  1. Initial lightning pain from root lesions
  2. Eventual loss of vibration, position sense and all sensory modalities of lower limb
  3. Areflexia and preserved strength

Etiology: Neurosyphilis

Can often see Charcot Joints

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8
Q

What are Charcot Joints? What disease are they associated with?

A

Severe, traumatic injury and deformation of ankle joints due to loss of sensation from Tabes Dorsalis

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9
Q

Describe the etiology (3), pathophysiology and presentation (3) of Brown-Sequard Syndrome

A

Pathophys: Spinal cord hemisection

Presentation:

  1. Contralateral STT deficit (loss of pain/temp)
  2. Ipsilateral CST deficit (muscle weakness)
  3. Ipsilateral Dorsal Column Deficit (vibration/position sense loss)

Etiology: Tumor (extramedullary); Trauma; Herniated disc

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10
Q

Describe the presentation of Myasthenia Gravis

Age? Symptoms? Affect on sensations/reflexes?

A
  1. Begins at any age
  2. 10-20% how just ocular MG (ptosis, diplopia only)
  3. 80-90% show general MG (Possible weakness of all muscles)- Ptosis, diplopia, neck/limb weakness, respiratory weakness, etc.
  4. Preserved sensations/reflexes
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11
Q

Pathogenesis of Myasthenia Gravis

A
  • Antibodies to AchR which competetively block receptors and increase their degeneration and turnover
  • Loss of this fxnal AchR leads allows even normal, mild reductions of Ach to lead to critical loss of end plate depolarization (and thus muscle fiber depolarization)
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12
Q

Dx and Tx of Myasthenia Gravis

A

Dx:

  1. Tensilon Test (edrophonium)- AchE inhibitor
  2. Clinical presentation
  3. EMG evidence of abnormal NMJ transmission
  4. Elevated AchR serum antibody

Tx:

  1. Ach drugs (Usually AchE inhibitors)
  2. Thymectomy (Autoimmunity is likely initiated in the thymus due to AchR like molecules)
  3. Immunosuppresants
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13
Q

Lambert-Eaton Syndrome

Presentation? Pathogenesis? What disease is it often associated with?

A

Pathogenesis: Autoimmune attacks against presynaptc calcium channels of the NMJ, leading to impaired Ach release.

Often arises as a paraneoplastic syndrome associated with Lung Small Cell Carcinoma

Presentation:

  1. Fatigable weakness of proximal limbs/trunk which mimics myopathy
  2. Weakness improves with use! (because there is more firing of nerves so more attempts at Ca2+ release so more antibody competition.
  3. Eyes are usually spared
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14
Q

Dx and Tx of Lambart-Eaton Myasthenic Syndrome (LEMS)

A

Dx: nerve stimulation tests, EMG, specific antibodies

Tx: Resection of the cancer; drugs which enhance Ach release (guanidine; 3,4-diaminopyridine)

AchE drugs are NOT EFFECTIVE! - Ach is never released in the first place

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15
Q

Mononeuropathy vs. Polyneuropathy

A

Mono: Injury to single, major, named nerve

Poly: Disorder of multiple, major and minor nerves (aka peripheral neuropathy)

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16
Q

What are the (2) main causes of mononeuropathy?

How is “focal demyelination” related?

A
  1. Trauma
  2. Compression

Focal demyelination is seen in locations where the nerve is being consistently compressed. It may be accompanied by axonal damage if the lesion is severe.

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17
Q

Describe the pathology of Carpal Tunnel Syndrome. How does it present (3)?

A

This is the most common mononeuropathy. It occurs when flexor tendons passing through the carpal tunnel get inflamed or swollen, compressing the median nerve.

Can also be caused by fluid retention in pregnancy.

Pt. presents w/ (1.) tingling/numbness in hand, (2) thenar weakness and (3) atrophy if severe.

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18
Q

What is wallerian degeneration? How does it relate to axonal sprouting?

A

Results from traumatic mononeuropathy. When a nerve fiber is cut or crushed, the part of the axon separated from the neuron’s cell body degenerates distal to the injury.

If the framework /scaffolding remains, axonal sprouting may progress, allowing a new axon to grow to the appropriate muscle. Otherwise surgery will be indicated.

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19
Q

What presentation is associated with polyneuropathy? (5)

A
  1. Stocking/glove sensory loss/impairment (feet first [longest sensory fibers], then hands)
  2. Paresthesia (spontaneous pins/needles)
  3. Dyesthesia (unpleasane sensation from a non-painful stimulus
  4. Distal limb weakeness/atrophy
  5. Declined reflexes
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20
Q

What are the (2) general processes of polyneuropathy? What test is helpful in differentiating them and how do we read it?

A
  1. Demyelination
  2. Axonal Degeneration

EMG aka Nerve conduction studies are useful in reading stimulated sensory and motor neurons.

Dec. nerve conduction velocity = Demyelination

Dec. amplitude = Axonal Degeneration

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21
Q

Pathophysiology of Guillain-Barre Syndrome.

Tx?

A

Pathophys- Inflammation and demyelination of peripheral nerves/roots (leading to ascending paralysis).

Tx: IVIG or plasmapheresis

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22
Q

How common is chronic, acquired polyneuropathy?

What are the top (4) causes?

A

This is the most common neuropathy

DM, cancer, infxn, or nutritional

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23
Q

What is the pathogenesis of hereditary neuropathy? Presentation? Tx?

A

Pathogenesis: Metabolic mechanisms or genetic disorders

Presentation:

  1. Childhood onset
  2. Distal sensorimotor deficits (little to no parasthesia/dysesthesia).
  3. Typically, orthopedic deformities are present (scoliosis, hammertoes, pes cavus aka high arch)

Tx: No curative treatment

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24
Q

What is a myopathy? What are the general Sx? Dx?

A

It is a primary disease of the muscle

Sx:

  1. Weakness, fatigue, cramps
  2. Proximal limb weakness/atrophy (shoulders, hips, and thighs)
  3. Late reflex loss
  4. Intact sensation

Dx:

Elevated serum muscle enzymes, biopsy, EMG

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25
Q

What is polymyositis? What is the most common cause?

A

It is inflammation and weakness of multiple muscles

It can be the result of viral infx or drug rxn, but most often a result of autoimmunity.

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26
Q

What is the presentation of polymyositis (2)? Dx? Tx?

A

Presentation:

  1. Proximal weakness over weeks/months
  2. Rash (dermatomyositis) around eyes/fingers

Dx: EMG, biopsy showing inflammation/muscle fiber necrosis

Tx: Corticosteroids or other immunosuppressants

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27
Q

Duchenne’s Muscular Dystrophy

How is it inherited? Pathophysiology? Presentation (including key signs)? Cause of death?

A

X-linked inheritance (so males only)

Pathophys: Loss of dystrophin- critical anchoring protein for muscle.

Presentation:

  1. Calf pseudohypertrophy (replacment of muscle by fat)
  2. Proximal weakness in young boys
  3. Hip gyrtle weakness requiring gower’s sign to stand
  4. Cardiorespiratory death by 3rd decade
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28
Q

Spinal Muscular Atrophy

Presentation/ Pathophysiology?

Infantile vs Childhood/Adult types?

A

Degradation involving anterior horn cells. Presents w/ LMN signs (weakness, atrophy, areflexia and fasiculations)

Infantile: Werdnig-Hoffman Disease- terminal condition due to rapid development of diffuse weakness, w/ no current curative treatment

Childhood/Adult: More mild; chronic disability

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29
Q

Amyotrophic Lateral Sclerosis

Pathophysiology? Tx? Prognosis?

A

Progressive degeneration of all UMN and LMNs (so symptoms are both upper and lower)

Tx: No cure; Riluzole (glutamate antagonist) prolongs survival by months

Prognosis: Fatal (50% die w/in 3 years from resp. failure or complications of profound weakness)

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30
Q

Most common cause of damage to the olfactory nerve (CN I)

A

Sinusitis or URI

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31
Q

What reflexes contribute to the near reflex? (3)

A

Lens accomodation + pupillary constriction + convergence

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32
Q

When can we see a dissociation of the light reflex and the near reflex? How does the dissociation work? Give specific examples.

A

This is when the pupil constricts w/ the near reflex but not w/ the light reflex

It is due to selective disruption of the light reflex pathway at the pretectal area.

Occurs in Neurosyphillis (Argyll Robertson’s pupil); Dorsal Midbrain Lesions (ex. Pineal tumors) –> Parinaud’s syndrome (if it also includes poor upgaze)

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33
Q

Pathophysiology for symmetrical vs asymmetrical nyastagmus

If lesions are present, where are they?

A

Symmetrical (all directions of gaze): usually drugs/ metabolic

Asymmetrical: anatomical lesion

Lesions are in vestibular system, brainstem or cerebellum. Somewhere, where they are upsetting control/balance of eye movements.

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34
Q

What is internuclear ophthalmoplegia and what pathologies do we see it with?

A

Breaking of coordinated lateral gaze, due to problem w/ MLF. May also see nystagmus of abducting eye.

Seen w/…

  1. MS in younger patient
  2. Ischemic infarct of older patient
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35
Q

Trigeminal Neuralgia

What is it?

Who does it happen to?

Tx.?

A
  • Short-circuiting nerve condition, causing lightning-jabs of pain (usually V2/V3).
  • Seen in young MS patients
  • Seen w/ tortuos blood vessels compressing nerve in older pts
  • Tx: Pain
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36
Q

UMN lesion has what affect on the muscles of mastication? LMN weakness?

A

UMN Lesions: Due to bilateral control of muscles of mastication, UMN lesions may cause jaw weakness but no deviation.

LMN Lesions: Jaw-deviation is seen

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37
Q

Other than facial drooping, what are some other effects of seering CN VII? (2)

A
  1. Loss of taste over ipsilateral anterior 2/3rds of tongue
  2. Ipsilateral hyperacusis (sensitivity to loud sound) due to loss of stapedius branch
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38
Q

UMN vs LMN damage to tongue innervation

A

UMN: contralateral genioglossus weakness and tongue deviation to opposite side

LMN: Weakness to ipsilateral tongue, atrophy, fibrillations, and fasiculations (you lick your wouds)

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39
Q

Weber Syndrome

  1. What is it?
  2. What causes it?
  3. How does it present? (2)
A
  1. It is a crossed brainstem syndrome of the medial midbrain
  2. Caused by occlusion of the posterior cerebral artery
  3. (1) ipsilateral CNIII damage; (2) contralateral hemiplegia (due to cerebral peduncle injury)
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40
Q

Wallenberg Syndrome

  1. Also known as what?
  2. What causes it?
  3. Clinical manifestations? (5)
A
  1. aka Lateral Medullary Syndrome
  2. Caused by occlusion of PICA
  3. I PP (on the) NHL:
  • Ipsilateral unless otherwise noted
  • Palatal/vocal weakness
  • Pain/temp loss (ipsi: face; contra: body)
  • Nystagmus
  • Horner’s
  • Limb dysmetria
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41
Q

Presentation: Sudden onset, worst headache of life, some neurological deficit.

Likely Dx:?

A

Aneurysmal Subarachnoid Hemorrhage

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42
Q

Presentation: Pt. has consistent headache and has been previously diagnosed w/ a coagulopathy or is taking anticoagulants.

Dx. to consider: ?

A

Dx: Subdural or intradural hematoma

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43
Q

What drug class should you avoid for pt’s w/ HA?

Give an example

A

Narcotics

Ex. Butalbital-acetaminophen

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44
Q

Are migraines usually unilateral or bilateral? When is the normal onset?

A

Unilateral

Onset: late childhood to early adult life (uncommon for first one in old age)

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45
Q

Name and describe the (4) Phases Migraines

A
  1. Prodrome: 6-48 hours prior to headache; depression, irritabilit, drowsiness, hunger/thirst, rhinorrhea/lacrimation
  2. Aura: usually visual; develop over 5-20 mins and lasts less than 60 mins; HA w/in 60 mins; due to spread of cortical depression
  3. Pain: associated w/ photophobia/phonophobia; N/V; thermophobia/osmophobia
  4. Postdrome: mood changes; impaired concentration; scalp/muscle tenderness
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46
Q

What is the basic path of effects that leads to migraine?

A
  1. NMDA activation
  2. Burst of focal cerebral activity
  3. Wave front w/ depression behind it moving at 3mm/min
  4. Trigeminal pathway triggered
  5. Release of neuropeptides leading to symptoms
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47
Q

Tx. of Migraine

A

Treat early and often

  1. NSAIDs (first line)
  2. Triptans (second line)
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48
Q

All triptans are agonists of…

What are potential SEs?

A

5HT 1B/D receptors

SE of vasoconstriction

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49
Q

Serotonin syndrome

A

Potential SE for pt given a triptan while on antidepressants

  • Severe rigidity (mostly legs)
  • Dysautonomia (inc. parasymp)
  • Encephalopathy (myoclonos, hyperreflexia, and seizures)
  • Usually w/in 24hr of med exposure
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50
Q

Cluster Headaches

  1. Who do they affect?
  2. Clinical presentation? (how often? for how long? uni or bi-lateral?)
  3. Tx?
A
  1. Men who are heavy smokers/drinkers
  2. Clusters last 6-12 weeks, every 1-2 years; rapid onset of 1-4 attacks for 15-30 min period; unilateral (but can bounce between sides)
  3. O2, injectable sumatriptan; nasal spray; lidocaine; DHE; prednisone
    1. Oral drugs not of much use given rapid time
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51
Q

Phonophobia/Photophobiain a Tension HA

A

You can have one or the other, but not both at the same time

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52
Q

Trigeminal Neuralgia

  1. What is it?
  2. What is the usual cause?
  3. Tx?
A
  1. Paroxysmal pain attacks that last from seconds to minutes
  2. Usually idiopathic, but MS is the most known cause for young people
  3. Tx: Carbamazepine (1st line)
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53
Q

Pseudotumor Cerebri

  1. Typical presentation?
  2. Dx?
  3. Tx?
  4. Potential outcome?
A
  1. Overweight, young, female, on oral contraceptives, and generalized headache
  2. Papiledema on fundoscope; Spinal tap to confirm high intracranial pressure (>250 mmH2O)
  3. Tx. w/ acetazolamide, topiramate, or surgical intervention
  4. Can lead to blindness if not caught
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54
Q

Primary Exertional Headache

  1. Presentation
  2. Tx
A
  1. Presentation: Young male w/ pulsating heading during/after physical activity
  2. Tx: beta blockers; indomethacin
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55
Q

Charcot’s Triad of MS

A
  1. Nystagmus
  2. Intention tremor
  3. Scanning Speech
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56
Q

Stereotypical patient for MS

A

Younger (20-50), white, female from the north

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57
Q

Describe the pathogenesis for MS

A
  1. APCs present neuronal tissue and prime autoreactive T-cells
  2. T-cells attach to, break down, and cross BBB
  3. T cells release interleukins causing inflammation; cytokines are released leading to myelin destruction
  4. Axons usual remyelinate but not well, eventually leading to axonal death and progessive degeneration
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58
Q

What are the (3) general syndromes which are highly suggestive of MS?

A
  1. Optic neuritis
  2. Brainstem syndromes (Including Internuclear Ophthalmoplegia – essentially pathognomonic for MS)
  3. Spinal cord syndromes
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59
Q

Describe the clinical manifestations of Optic Neuritis (associated syndrome of MS) (5)

A
  1. Decreased monocular vision
  2. Pain w/ eye movement
  3. Decreased red/green color
  4. Afferent pupillary defect
  5. Heat intolerance
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60
Q

What is Lhermitte’s “sign”, and what is it associated with?

A

Lhermitte’s “sign” is an electric sensation felt by the patient when the neck is flexed (“sign” because it is actually a symptom). Associated spinal cord syndrome (which is suggestive of MS)

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61
Q

What is a key point about location of a plaque on MRI when it comes to MS?

A

In MS, plaques are found right against the pia surface

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62
Q

In MS cases, what does a black hole on T1 MRI tell us?

A

It is a sign of atrophy/ chronic damage

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63
Q

What is this image and what disease is it associated with?

A

Dawson’s fingers

Pathognomonic for MS

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64
Q

What is the tract most commonly involved when there is an MS plaaque on the SC?

A

DSC

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65
Q

Neuromyelitis Optica

  1. Pathophysiology
  2. Associated symptoms
  3. Dx
  4. Prognosis
A
  1. Longitudinal, extensive, spinal cord lesion (>3 vertebral segments)
  2. Bilateral optic neuritis. Hicups, and normal/minimal brain lesions
  3. NMO IgG Ab positive
  4. Much worse prognosis
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66
Q

Acute Disseminated Encephalomyelitis (ADEM)

  1. What is this disease process associated with?
  2. Presentation?
  3. View on MRI
  4. What patient population does this occur in?
A
  1. Post-infectious process; differential for MS
  2. One time process which commonly presents w/ HA, N/V, drowsiness and meningism
  3. Large, fluffy, multifocal lesions
  4. More common in children than adults
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67
Q

Progressive Multifocal Leukoencephalopathy (PML)

  1. Pathology?
  2. What conditions/virus is it associated with?
  3. How is it related to MS?
  4. How does it classically look on MRI?
  5. How does it look on histology?
A
  1. Multiple lesions frequently in subcortical hemispheric white matter or cerebellar peduncles
  2. Associated with JC virus and the immunocompromised
  3. Rare SE that occurs in those who are JC positive and on natalizumab, an MS drug
  4. Hyperintense FLAIR signal in the right cerebellar peduncle is classic
  5. Histology shows: loss of myelin (w/axonal sparing), bizarre astrocytes, ground glass oligodendroglial inclusions.
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68
Q

MS Tx

A
  • IV steroids are the preference (methylprednisonle) or oral prednisone can be given
  • ACTH, Plasmapharesis, IVIg
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69
Q

What is encephalitis ( and meningoencephalitis) and what is the usual cause?

A

Infxn of the brain parenchyma (w/ accompanying meningitis in the case of meningoencephalitis)

Mostly caused by viruses

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70
Q

Most common pathogens for acute bacterial meningitis for ages:

1-12 months

A

: E. Coli, Group B Strep

1-12 months: S. Pneumo, H. Flu (if unvaccinated)

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71
Q

Most common pathogens for acute bacterial meningitis for ages:

12 mo -16 y/o

16-50 y/o

Age extremes

A

12 mo- 16 y/o: N. meningitis, H. flu, S. pneumo

16 - 50 y/o: S. pneumo, N. meningitis

Age extremes: L. monocytogenes; Pseudomonas

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72
Q

Who is commonly affected by fungal meningitis?

A

The immunocompromised

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73
Q

Expected CSF findings for Bacterial meningitis:

  1. Fluid quality?
  2. Type of cells present?
  3. Protein quantity?
  4. Glucose levels (relative to plasma)?
  5. Pressure?
A
  1. Fluid quality? Cloudy
  2. Type of cells present? PMN’s
  3. Protein quantity? Very high
  4. Glucose levels (relative to plasma)? Low
  5. Pressure? High
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74
Q

Expected CSF findings for Viral Meningitis:

  1. Fluid quality?
  2. Type of cells present?
  3. Protein quantity?
  4. Glucose levels (relative to plasma)?
A
  1. Fluid quality? Clear
  2. Type of cells present? Lymphs
  3. Protein quantity Slightly High
  4. Glucose levels (relative to plasma)? Normal
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75
Q

Expected CSF findings for TB Meningitis:

  1. Type of cells present?
  2. Protein quantity?
  3. Glucose levels (relative to plasma)?
A
  1. Type of cells present? Lymphs
  2. Protein quantity? Moderate
  3. Glucose levels (relative to plasma)? Mildly Low
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76
Q

Tx of bacterial meningitis

A

IV steroids + antibiotics

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77
Q

In TB meningitis, where is the exudate normally found?

A

The base of the brain

78
Q

Expected CSF findings for Fungal Meningitis:

  1. Type of cells present?
  2. Protein quantity?
  3. Glucose levels (relative to plasma)?
A
  1. Type of cells present? Lymphs
  2. Protein quantity High
  3. Glucose levels (relative to plasma)? Low
79
Q

(4) potential complications of bacterial meningitis

A
  1. Hydrocephalus due to pus obstructing CSF outflow
  2. Infarction from thrombosis of inflamed superficial vessels of cortex/SC
  3. Deafness in children
  4. Secondary Edema and Inflammation of cortex (meingoencephalitis)

HIDE from meningitis

80
Q

What are the (3) main types of parasitic infxns? Which is most common?

A
  1. Cysticerosis (from Taenia Solium) * most common
  2. Toxoplasmosis
  3. Amoebiasis ( N. fowleri, E. histolytica, etc.)
81
Q

What are the key causes of viral meningitis/encephalitis in the…

Summer/early fall?

Any season?

A

Summer/early fall- Enteroviruses * and arboviruses** (west nile)

Any season- Herpes simplex virus

* most common cause

** most common cause in USA

82
Q

What are the (4) key microscopic findings in viral encephalitis?

A
  1. Perivascular inflammation
  2. Leptomenigeal inflammation
  3. Microglial clusters (aka nodules)
  4. Neuroplagia
83
Q

Polioencephalitis

  1. Transmission?
  2. Pathogenesis?
  3. Dx?
  4. Similar to the pathology of what virus?
A
  1. Fecal-oral transmission
  2. Infxn and subsequent destruction of anterior horn cells (LMN)
  3. Virus recovered from stool or throat
  4. WNV
84
Q

What is this image and what pathological process is it affliated with?

A

It is a negri body (cytoplasmic inclusion), seen in a neuron of the brainstem, cerebellum, or hippocampus.

Associated with Rabies

85
Q

Herpes Encephalitis

  1. Caused by what virus?
  2. Transmission
  3. Acute phase?
  4. Chronic phase?
  5. Sx?
  6. Tx?
A
  1. HSV-1
  2. Transmitted via saliva
  3. Acute- Focal Encephalitis- Bilateral but assymetrical edema, hemorrhage, and necrosis in the temporal or frontal lobes.
  4. Chronic- “burnt-out” herpes-encephalitis
    • Progression to cavitation and atrophy for long-term survivors
  5. Sx: Aphasia, Behavorial changes, Memory impairment
  6. Tx: w/ acyclovir
86
Q

You see a “bullet-shaped” Rhabdovirus on EM. What disease do you suspect?

A

Rabies

87
Q

What is this and what disease process is it associated with?

A

HSV-1 Intranuclear Inclusions (Owls-eye)

Herpes Encephalitis

88
Q

What are the TORCH diseases?

A

TOxoplasma

Rubella

CMV

Herpes simplex

Can all be transmitted to the fetus

89
Q

Congenital CMV Encephalitis vs CMV Postnatal infxn

A

Congenital: Moderately dilated ventricles and several foci of calcifications in the periventricular region. Lots of cytomegalic inclusions in all cellular elements of the brain

Postnatal infxn: numerous microglial nodules, only occasional cytomegalix cells with inclusions

90
Q

HIV Encephalitis (HIVE) vs HIV Leukoencephalopathy

A

HIVE: Wide spread Multinucleated giant cells + microglial nodule (pathognomonic for HIV encephalitis)

HIV leukoencephalopathy: Subacute HIVE + onset of cognitive impairment and apathy (potentially leading to AIDS dementia).

91
Q

What pathology is this image associated with?

A

Microglial nodule + multinucleated giant cell = HIVE

92
Q

Vacuolar myelopathy

  1. What is it?
  2. What is it similar to?
  3. Sx? (3)
A
  1. Vacuoloation of the posterior and lateral spinal columns.
  2. SImilar to Subacute Combined Degeneration seen in B12 def.
  3. Spastic paraparesis + hyperreflexia + ataxia
93
Q

Where are brain abscesses usually found?

A

In areas of the brain where the collateral circulation is the poorest (least blood flow).

94
Q

Describe the Evolution of an Abscess

  1. Initiating action
  2. Days 1-3
  3. Days 2-7
  4. Days 5-14
  5. 2 weeks +
A
  1. Injury to micro-vasculature and spread of bacteria across the wall of the injured blood vessel
  2. Early cerebritis
  3. Confluent necrosis
  4. Early encapsulation
  5. Late encapsulation
95
Q

What are the (2) main stages of Alcohol toxicity? Tx?

A
  1. Early hypersympathetic stage (tremors, sweating, tachycardia) and general seizures (12h to 3 days after withdrawal begins)
  2. Delirium tremens w/ fluctuating motor and autonomic acitivity, confusion and hallucinations

Tx: Benzos

96
Q

Name/describe the main chronic alcoholism syndromes (4)

A
  1. Wernicke’s- TACO: Thiamine deficiency; AMS; Cerebellar dysfxn; Occulomotor Dysfunction
  2. Korsakoff- amnesia, confabulation
  3. Alcholic cerebellar degeneration
  4. Peripheral neuropathy
97
Q

Prion Disease

  1. What is it?
  2. Most common types?
  3. Sx/Prognosis
A
  1. Infxs proteins which induce conformational changes in normal proteins. Leads to neuronal death in the absence of inflammation.
  2. Most common is Creutzfeldt-Jakob; Mad cow is next most common (bovine spongiform encephalopathy)
  3. Sx: dementia w/ myoclonus (often corticospinal) Prognosis: Rapidly progessive, untreatable, fatal
98
Q

Optic atrophy

  1. Occurs when?
  2. What does the optic disc look like?
  3. What is it result of?
A
  1. Occurs weeks after an optic nerve lesion
  2. Pale optic disc w/ sharp, distinct images
  3. Result of destruction of retinal ganglion cell axons (not an occiptal lesion)
99
Q

Pituitary Lesion

Describe the pathology and clinical presentation

A

This tumor compresses the center of the optic chiasm from below, taking out superior vision loss and the eventually will cause bitemporal hemiopsia.

100
Q

Major effect of occlusion of the PCA

A

Cortical blindness due to bilateral occipital infarcts

101
Q

Conductive deafness and Nerve deafness

Which is high tone? Which is low tone?

A

Conductive deafness: low tone (impacted wax; ossicle lesion)

Nerve deafness: high tone

102
Q

Benign Positional Vertigo

  1. Common in who?
  2. Pathology?
A
  1. Elderly
  2. Degenerated otoliths w/ Ca2+ crystals lodged over cilia so minor movements of head creates vertigo sensations
103
Q

Acute labyrinths

A

Viral infxn or inflammation of inner ear labyrinth which leads to asymmetrical nystagmus, unilateral hearing loss, and gait ataxia on exam

104
Q

Meneire’s disease

A

Membranous labyrinth swells/ruptures

Intermixed endo- and peri-lymph impairs receptors

Permanent deafness may occur after repeated bouts

RARE

105
Q

Put these cells in order of most to least sensitivity to ischemia

oligodendrocytes, astrocytes, neurons, endothelial cells

A
  1. neurons
  2. oligodendrocytes
  3. endothelial cells
  4. astrocytes
106
Q

What are the (4) major etiologies of Global ischemia?

A
  1. Low perfusion
  2. Acute drop in BF
  3. Chronic hypoxia (anemia)
  4. Repeated episodes of hypoglycemia (insulinoma)
107
Q

Histological changes in first 6-12 hours after an infarct

A

Red Dead Neurons

  1. Cytoplasmic eosinophilia
  2. Loss of Nissl substance
  3. Dark pyknotic nuclei1
108
Q

Key watershed areas for brain infarcts (3) in adults

In children?

A

Adults:

  1. Pyrimadal neurons in cerebral cortex (Laminar necrosis)
  2. Pyrimadalneurons in hippocampus
  3. Purkinje cells of cerebellum

Infants:

Thalamus and Pons

109
Q

A dominant hemisphere MCA infarct is often associated with…?

A non-dominant?

A

Dominant: Expressive aphasia

Non-dominant: Neglect

110
Q

Are lacunar infarcts are usually the result of embolisms or in-situ thrombosis?

A

In-situ

111
Q

General Etiologies for hemorrhage above the arachnoid? Below?

A

Above: Trauma

Below: Underlying cerebrovascular disease (Subarachnoid - Berry Aneurysm) or (Parenchyma- HTN)

112
Q

Top (2) locations for Berry Aneurysms

A
  1. ACA
  2. MCA
113
Q

Most common cause for subarachnoid hemorrhage? Second most common cause?

A
  1. Trauma
  2. Berry-aneurysm
114
Q

Intraventricular Hemorrhage is most common in who? Most common where?

A
  1. Common in premies
  2. Germinal matrix (beneath the ependyma)
115
Q

Duret Hemorrhages are caused by…?

A

Secondary compression from herniation of the medial temporal lobe, leading to stretching and ischemia of perforating arterioles

116
Q

Most artery involved in epidural hemorrhage? Most common mechanism of injury?

Talk and die or progressive?

A

Classically due to a temporal bone fracture w/ rupture of the middle menigeal artery

(MMA fighters have epidural bleeds)

Talk and die

117
Q

Subdural Hematoma

Talk and die or progressive? What vessels are the usual cause?

A

Progessive decompensation

Usually casued by bridging veins rupture

118
Q

Describe the (3) main herniation types and their potential consequences

A
  1. Tonsilar: Displacement of cerebellar tonsils into foramen magnum; Compression of brainstem and subsequent Cardiopulmonary arrest
  2. Subfalcine: Displacement of cingulate gyrus under falx cerebri; Compression of ACA leading to infarction
  3. Uncal: Displacement of medial temporal lobe under tentorium cerebri; POP: Paramedian vessel rupture (duret), Oculomotor compression, PCA compression
119
Q

ARAS

A

Ascending reticular activating system

120
Q

When testing a patient in a coma, what does the following sign suggests?

  • Withdrawal from painful stimuli
A

Some remaining cortical function

121
Q

When testing a patient in a coma, what does the following sign suggests?

(Reflexive movement to pain test)

Decorticate posturing

Decerebrate posturing

A

Decorticate- Cerebral hemisphere lesion

Decerebrate-Lesion in midbrain (red nucleus)

122
Q

When testing a patient in a coma, what does the following sign suggests?

(Breathing patterns)

Cheyne-stokes

Ataxic, irregular respiration

A

Cheyne-Stokes: due to bilateral cortical lesions

Ataxic-irregular: lesion near respiratory center (impending resp. failure)

123
Q

When testing a patient in a coma, what does the following sign suggests?

Pupillary light reflex

A

Brainstem is intact at least at level of midbrain

124
Q

When testing a patient in a coma, what does the following sign suggests?

Oculocephalic reflex

Oculovestibular reflex

A

Occulocephalic (doll’s eye): intact brainstem

Oculovestibular (ice water in ear canal- eyes move towards cold water): intact brainstem

125
Q

After checking for ABC’s, what is my next critical step for tx. of a coma patient in an emergent situation?

A

Immediately check hypoglycemia or give 50% IV dextrose

126
Q

How long most cerebral blood flow be abscent to qualify a patient as having brain death?

A

Absent cerebral blood flow over 10 mins

127
Q

What is the etiology of hemiballismus?

A

Lesion of the Subthalamic Nucleus (STN), which normally stimulates the GPm

128
Q

Primary and secondary clinical of parkinsons

A

PARK HAM

Primary: Pill rolling tremor, Areflexia postural reflexes, Rigidity, Kinesia(brady)

Secondary: Hypophonic speech, Autonomic dysfxn, Micrographia

129
Q

What is the relationship between CO poisoning/ manganese poisoning and parkisons disease

A

Poisoning from these substances can lead to parkisonism

130
Q

Clinical Dx of Parkinson’s disease (4)

A
  1. > or equal to 2 primary clinical signs
  2. 40-70 y/o
  3. Exclusion of other causes
  4. Initial signficant improvement w/ dopaminergics
131
Q

What are Lewy bodies and how are they related to Parkinson’s?

A

They are eosinophilic, intraneuronal cytoplasmic inclusions which are an accumulation of a-synuclein (synucleinopathy).

Seen in advanced parkinson’s. Some families have a-synuclein and/or parkin mutations increasing susceptibility to parkinson’s.

132
Q

Parkinson’s Tx (3)

A
  1. L-Dopa (+ Carbidopa)
  2. Pallidotomy (destruction of GPm)
  3. STN stimulator (actually serves to inhibit STN and thus inhibits GPm)
133
Q

What does the CT show for Huntington’s patients?

A

Atrophy of caudate nuclei and cerebral cortex

134
Q

What is the genetic abnormality for Huntington’s disease? (including the chromosome which is abnormal)

A

Trinucleotide repeats of Huntington gene at chromosome 4 (>35 CAG repeats)

135
Q

What are the early onset genetic changes for Alzheimer’s? Late onset? Protective?

A

Early: Down’s Syndrome, Presenilin 1/2 (chromosome 14/1)

Late: ApoE4

Protective: ApoE2

136
Q

Alzheimer’s and Amyloid

A

Abnormal cleavage of Amyloid precursor proteins leads to excess accumulation of amyloid.

137
Q

Where are the earliest signs of Alzheimer’s often seen in the anatomy?

A

Hippocampus

138
Q

Neurofibrillary Tangles (NFT)

(what are they? what kind of proteins? what does it correlate with?)

A
  • Intracellular filamentous inclusions
  • Hyperphosphorylated tau protein
  • Density correlates w/ degree of dementia
139
Q

Amyloid angiopathy

A

Amyloid deposition in walls of arterial vessels in subarachnoid space, that separates media and adventitia. Present in almost all AD cases

140
Q

What are the top (3) causes of dementia?

A
  1. Alzheimer’s
  2. Lewy Body Disease
  3. Frontotemporal Lobar Degeneration (Of which Pick’s disease is a subset)
141
Q

Lewy Body Disease

Describe the Pathophys and the Sx’s

A
  1. Lewy bodies composed of a-synuclein in cortex and brainstem
  2. Initial dementia and visual hallucinations followed by parkinsonian symptoms
142
Q

Frontotemporal Lobar Degeneration

  1. Pathophys? (key chromosome involved?)
  2. Presentation?
  3. Key disease under this umbrella
A
  1. Mutations in tau protein gene in chromosome 17 leading to breakdown of the frontal and temporal lobes
  2. Changes in personal and social conduct
  3. Pick’s disease is a subset
143
Q

Pick’s Disease

  1. What is this disease a subset of?
  2. Presentation?
  3. What are Pick’s Bodies, what are they composed of, and where are they found?
A
  1. Rare type of frontotemperal dementia
  2. Aphasia (w/ minimal memory loss); can lead to dementia
  3. Pick’s Bodies- Globose neuronal cytoplasmic inclusions composed of tau and found in the hippocampus and cortex
144
Q

What are the systems affected in multisystem atrophy? What is the pathology?

A
  1. COPS: Cerebellum (leading to ataxia), Olivary and Pons (leading to autonomic dysfunction), Substantia Nigra (leading to Parkinsonism)
  2. Glial Lewy bodies
145
Q

What is the genetic mutation associated with familial ALS?

A

Mutation on the gene for Superoxide Dismutase (SOD1)

146
Q

Werdnig-Hoffman Disease

  1. Mode of inheritance
  2. Pathology
  3. Presentation
A
  1. Autosomal recessive SMAI defect on Chromosome 5
  2. Degeneration of LMNs and atrophy of distal muscles
  3. “Floppy baby syndrome” (affects fetus/neonate)

(sick before they can say their first “werd”)

147
Q

Kugelberg-Walander Disease

  1. Key genetic mutation
  2. Similar to what disease?
  3. Prognosis?
A
  1. SMA II mutation at chromosome 5
  2. Similar to Werdnig-Hoffmann but presents after 3mo
  3. Chronic – compatible with normal life span
148
Q

Freidrich’s Ataxia

  1. Most common form of…?
  2. Describe the genetic issue
  3. What neural components are degenerated?
A
  1. Most common hereditary ataxia
  2. Trinucleotide repeat of GAA at chromosome 9
  3. freidriCH’S​​
    • Cerebellum (ataxia)
    • Heart (electrical conduction and structural anomalies)
    • Spinal (vibration loss)
149
Q

Vascular Dementia

  1. This is ultimately just a product of what?
  2. What other dementia process is this closely associated with?
  3. What genetic changes can be associate?
  4. What is the most common genetic form of this disease and what arteries does it involve?
A
  1. Loss of blood flow to tissues (could be ischemic infarcts, hemorrhagic infarcts, hypoperfusion, amyloidosis leading to hemorrhage, etc.)
  2. Associated w/ mixed dementia (Alzheimer’s disease + vascular dementia)
  3. ApoE4 increases risk.
  4. CADASIL is most common genetic form, involving small vessels
150
Q

What effect does Wenicke’s encephalopathy have on mamillary bodies? (Acutely? Chronically?)

A

Acute: Mammillary body w/ petechial hemorrhages

Chronic: shrunken mamillary bodies

151
Q

Methanol toxicity vs CO poisoning

  1. MOA for methanol toxicity
  2. Type of injury seen in each
  3. Location of injury for each
A
  1. Methanol: Liver oxidation of methanol to formaldehyde and formic acid
  2. Hypoxic injury w/ white matter necrosis/ hemorrhage
  3. Methanol: Affects putamen and claustrem; CO: bilateral globus pallidus
152
Q

Central Pontine Myelinosis is caused by

A

Triangular lesion w/ myelin loss due to rapid correction of electrolyte imbalance for alcoholics

153
Q

Name the most common Primary Brain Tumors for an Adult.

Child?

A

Adult: (Gates Miliennium Scholar) Glioblastoma, Meningioma, Schwannoma

Child: Med-PEds

Medulloblastoma, Pilocytic astrocytoma, Ependymoma

154
Q

Grades for Astrocytoma and key tumors associated (4)

A

Grade I: Least malignant, slow growing, possible to cure w/ resection. Juvenile Pilocytic Astrocytoma

Grade II: Infiltrative/ recurrent, but no mitosis, necrosis, or angiogenesis

Grade III: Malignant but no microvascular proliferation/ necrosis (give radiation/ chemo)

Grade IV: Most malignant CNS tumor type. Fatal outcome. Glioblastoma

155
Q

Key histological presentation Juvenile Pilocytic Astrocytoma

  1. Cell type?
  2. Architecture?
  3. Type of fibers?
  4. Classic finding on MRI?
A
  1. Piloid cells w/ hair like processes
  2. Biphasic architecture (compact and microcytic areas)
  3. Rosenthal fibers
  4. On MRI - Cyst w/ mural nodule
156
Q

Tumor marker for Glioblastoma

A

(+) GFAP

157
Q
  1. What primary brain cancer does this image pertain to?
  2. Normal location for this cancer?
  3. Describe the expected Histo
A
  1. Oligodendroglioma (intratumoral calcifications on CT)
  2. Usually frontal lobe
  3. Fried-egg appearance (perinuclear halos); Chicken-wire capillary pattern
158
Q

In a rosette, what type of cancer has a core of…

  1. Neuropil fibrils (homer-wright)
  2. Empty lumen
  3. Blood vessels
  4. Empty central sulcus
A
  1. Medullablastoma
  2. Retinoblastoma
  3. Ependymoma (pseudorosette)
  4. Ependymoma (true rosette)
159
Q

Where is an Ependymoma most common?

A

They arise from the ventricle walls/ central canal of the SC. 4th ventricle is the most common site

160
Q
  1. What cancer is this image associated with?
  2. What type of cells does it arise from/ where in the brain?
  3. How does it spread?
A
  1. Medullablastoma
  2. Arises from undifferentiated neuroectodermal cells in the cerebellum of kids; cerebrum (hemispheric) of adults.
  3. Spreads along CSF pathways (so can be seen discretely on an MRI)
161
Q

Whorls, Psammoma bodies, Fasicles and a Dural tail, are all associated with what cancer? What specific cell type does this cancer grow from?

A

Meningioma

(Arachnoid layer)

162
Q
  1. What cancer is this image associated with?
  2. What population is most commonly affected?
  3. What is this often confused with?
  4. What embryological pouch does this develop from?
A
  1. Craniopharyngioma
  2. Children
  3. Pituitary adenoma
  4. Rathke’s pouch
163
Q

Schwannoma

  1. Where does this most commonly occur/what happens?
  2. What (2) related processes lead to it?
  3. What does it stain with?
A
  1. Cerebellopontine angle (where cranial nerve VIII runs). Leads to acoustic neuroma.
  2. Neurofibromatous Type 1 and Type 2
  3. Stains for S100 protein
164
Q

What gene is involved w/ NF1? NF2?

A
  1. NF1: 17q11.2
  2. NF2: 22q12
165
Q

What is this and what disease is this pathognomonic for? How does it look on gross.

A

Plexiform neurofibroma: tumor involving multiple nerve fasicles. Looks like bag of worms on gross

(seen in NF1)

166
Q

What (2) genes are associated w/ tuberous sclerosis?

A
  1. TSC1 (9q) - hamartin
  2. TSC2 (16p)- tuberin
167
Q

Classic triad for Tuberous Sclerosis

Other key presentations and important

A
  1. Seizures
  2. Adenoma sebaceum
  3. Mental retardation

SAM had Tuberous Sclerosis

Involves Tubers (even on face) and SEGAs (subependymal giant cells which can lead to hydrocephalous)

168
Q

What disease is this image associated w/? Explain. What chromosome is affected?

A

VHL disease (loss of tumor suppressor on chromosome 3)

CNS Hemangioblastoma (closely arranged thin-walled capillaries which can rupture)

169
Q

Tabetic gait

(what is it? what causes it?)

A

Foot slapping gait, where patient compensates for impaired sensation by forcibly planting foot down.

Due to neurosyphilis or severe neuropathy

170
Q

Waddling gait

(what is it? what causes it?)

A

When walking, weak pelvic/hip muscles cannot support the body “on one leg”, so patient compensates.

Usually the result of a myopathy

171
Q

Scissors gait

(what is it? what causes it?)

A

Weak legs but have spasms in adductor muscles forcing the knees stiffly together when walking

Due to CST lesion

172
Q

Festination

A

Leaning further and further to walk (Parkinson’s)

173
Q

Kinetic tremor vs Dysmetria

A

Kinetic: rhythmic oscillations during limb movement towards a target

Dysmetria: Overshooting or undershooting a target

174
Q

Dystonia vs myoclonus

A

Dystonia: Frequent, constant contraction

Myoclonus: Shock-like jerking or twitches

175
Q
  1. Where would a lesion be that causes Wernicke’s aphasia?
  2. Broca’s?
  3. What additional sign would expect?
A
  1. Wernicke’s: Posterior, superior temporal
  2. Broca’s Posterior, inferior frontal
  3. Hemiparesis would also be expected in damage to these areas because of proximity to motor cortex. (no hemi? suggests psychosis/drug use)
176
Q

Where would a lesion be that causes conductive aphasia?

How does it present?

A

Arcuate fasiculus (tract between Broca’s and Wernicke’s)

Intermediate versions of both (particuarly Wernicke’s)

177
Q
  1. What deficits would a posterior, D__ominant hemisphere lesion lead to?
  2. Non-dominant hemisphere lesion?
A
  1. Dominant: alexia (impaired reading); agraphia (impaired writing)
  2. Non-dom: aprosodies (semantic understanding)
178
Q

Lesions at what (3) locations lead to memory issues?

A
  1. Hippocampus
  2. Mamillary bodies
  3. Thalamus
179
Q

Where would a lesion be to cause gait apraxia? constructional or dressing apraxia?

A

Gait: prefrontal/frontal

Construction/dressing: Parietal

180
Q

Agnesia

(what is it? what causes it?)

A
  • Impaired recognition of perceived stimuli via one sensory modality (ex. can see it and not recognize, but hear it and know)
  • Due to lesion in sensory association cortex
181
Q

What is paratonia?

In what syndrome do you see both Paratonia and frontal lobe release signs?

A
  1. Frontal lobe release signs (normally seen in infancy)
  2. Paratonia: Resistance to rapid passive movement of a limb. Seen in frontal lobe syndrome

Frontal Lobe Syndrome

182
Q

Kluver-Bucy is caused by what lesion type?

A

Bi-temporal

183
Q

Parietal Lobe’s main functioning?

A

Sensory

184
Q

Anton’s Syndrome?

Prosopagnosia?

Both are the result of what?

A

Anton’s: Denial or unawareness of cortical blindness

Prosopagnosia: Inability to recognize previously known faces

Both are the result of bilateral occipital lesions

185
Q

Name the (3) types of partial seizures

A
  1. Simple Partial (focal w/o LOC)
  2. Complex Partial (focal + LOC)
  3. Partial + secondary generalized (focal then generalized)
186
Q
  1. Most common partial seizure
  2. What are the preceeding symptoms?
  3. What does the seizure look like?
A
  1. Temporal Lobe
  2. Epigastric Aura (rising sensation, fear, deja vu, olfactory, and gustatory sensations)
  3. Staring, unresponsiveness, oroalimentry, and gestural automatisms
187
Q

Frontal Lobe Seizures

  1. Timing?
  2. Types of movements (2)?
  3. Focal seizure patterns (2)?
A
  1. Usually at night
  2. Complex movement + Versive movements (head/eye rolling to opposite side of seizure)
  3. Focal seizure w/ Jacksonian March (through homonchulous) + Post-ictal “Todd’s” Paralysis
188
Q

Tx. of Absence seizures

A

Ethosuximide

189
Q
  1. What is a myoclonic seizure?
  2. When does it happen?
  3. Tx.?
A
  1. Fast, shock-like contraction
  2. Early in the morning for teenagers (often after alcohol use/ sleep deprivation)
  3. Tx. Valproic acid
190
Q

Tonic vs Clonic

A
  • Tonic- contraction producing extension/arching
  • Clonic- Alternating contraction/relaxation
191
Q

If you wanted to treat a child with febrile seizures (although you don’t need to).

A

Rectal Diazpam

192
Q

Status Epilepticus

  1. What is it?
  2. Treatment?
A
  1. NEUROLOGICAL EMERGENCY
    • Continuous seizures (> 5min, neural death > 30 min)
    • Greater than (2) seizures in a row w/o regaining of conciousness
  2. Tx:
    • Glucose check (consider thiamine)
    • Lorazepam
    • Phenytoin
    • ICU admission (Propofal or IV medazlin)

MHD2 Neuro (22 decks)

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